BioProject

Type 2 diabetes is recognized as one of the primary contributors to cardiovascular diseases, with vascular endothelial dysfunction (VED) being a crucial mechanism underlying its development. More...

Type 2 diabetes is recognized as one of the primary contributors to cardiovascular diseases, with vascular endothelial dysfunction (VED) being a crucial mechanism underlying its development. In this study, we present the aberrant expressions of CircHMGCS1 and miR-4521 in diabetes-induced VED. Overexpression of CircHMGCS1 or silencing of miR-4521 expedited the onset of diabetes and aggravated VED. Mechanistically, CircHMGCS1 upregulated ARG1 by sequestering miR-4521, resulting in the inhibition of vascular NO secretion, enhanced adhesion molecules expression of VCAM1, ICAM1, ET-1, and increased ROS generation. Consequently, these events accelerated the impairment of vascular endothelial function. These findings underscore the physiological roles of CircRNA and miRNA in cardiovascular diseases triggered by diabetes and suggest that modulating the expression of CircHMGCS1 and miR-4521 could serve as a potential strategy for preventing endothelial cell dysfunction and the development of diabetes-associated cardiovascular diseases. Overall design: In order to simulate the regulatory effect of diabetes on non-coding RNA in vascular endothelium in vitro, We used Human Umbilical Vein Endothelial Cells (HUVECs) to culture them in high fat/high glucose (PAHG) medium for 24h, and The medium contained 25 mM glucose and 250 μM saturated free fatty acid (FFA) palmitate were repeated three times, followed by total RNA extraction for RNA-SEQ analysis Less...